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Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation
A mutual interplay exists between adaptive immune system and gut microbiota. Altered gut microbial ecosystems are associated with the metabolic syndrome, occurring in most obese individuals. However, it is unknown why 10–25% of obese individuals are metabolically healthy, while normal weight individ...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479914/ https://www.ncbi.nlm.nih.gov/pubmed/28690599 http://dx.doi.org/10.3389/fmicb.2017.01157 |
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author | Pindjakova, Jana Sartini, Claudio Lo Re, Oriana Rappa, Francesca Coupe, Berengere Lelouvier, Benjamin Pazienza, Valerio Vinciguerra, Manlio |
author_facet | Pindjakova, Jana Sartini, Claudio Lo Re, Oriana Rappa, Francesca Coupe, Berengere Lelouvier, Benjamin Pazienza, Valerio Vinciguerra, Manlio |
author_sort | Pindjakova, Jana |
collection | PubMed |
description | A mutual interplay exists between adaptive immune system and gut microbiota. Altered gut microbial ecosystems are associated with the metabolic syndrome, occurring in most obese individuals. However, it is unknown why 10–25% of obese individuals are metabolically healthy, while normal weight individuals can develop inflammation and atherosclerosis. We modeled these specific metabolic conditions in mice fed with a chow diet, an obesogenic but not inflammatory diet—mimicking healthy obesity, or Paigen diet—mimicking inflammation in the lean subjects. We analyzed a range of markers and cytokines in the aorta, heart, abdominal fat, liver and spleen, and metagenomics analyses were performed on stool samples. T lymphocytes infiltration was found in the aorta and in the liver upon both diets, however a significant increase in CD4+ and CD8+ cells was found only in the heart of Paigen-fed animals, paralleled by increased expression of IL-1, IL-4, IL-6, IL-17, and IFN-γ. Bacteroidia, Deltaproteobacteria, and Verrucomicrobia dominated in mice fed Paigen diet, while Gammaproteobacteria, Delataproteobacteria, and Erysipelotrichia were more abundant in obese mice. Mice reproducing human metabolic exceptions displayed gut microbiota phylogenetically distinct from normal diet-fed mice, and correlated with specific adaptive immune responses. Diet composition thus has a pervasive role in co-regulating adaptive immunity and the diversity of microbiota. |
format | Online Article Text |
id | pubmed-5479914 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54799142017-07-07 Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation Pindjakova, Jana Sartini, Claudio Lo Re, Oriana Rappa, Francesca Coupe, Berengere Lelouvier, Benjamin Pazienza, Valerio Vinciguerra, Manlio Front Microbiol Microbiology A mutual interplay exists between adaptive immune system and gut microbiota. Altered gut microbial ecosystems are associated with the metabolic syndrome, occurring in most obese individuals. However, it is unknown why 10–25% of obese individuals are metabolically healthy, while normal weight individuals can develop inflammation and atherosclerosis. We modeled these specific metabolic conditions in mice fed with a chow diet, an obesogenic but not inflammatory diet—mimicking healthy obesity, or Paigen diet—mimicking inflammation in the lean subjects. We analyzed a range of markers and cytokines in the aorta, heart, abdominal fat, liver and spleen, and metagenomics analyses were performed on stool samples. T lymphocytes infiltration was found in the aorta and in the liver upon both diets, however a significant increase in CD4+ and CD8+ cells was found only in the heart of Paigen-fed animals, paralleled by increased expression of IL-1, IL-4, IL-6, IL-17, and IFN-γ. Bacteroidia, Deltaproteobacteria, and Verrucomicrobia dominated in mice fed Paigen diet, while Gammaproteobacteria, Delataproteobacteria, and Erysipelotrichia were more abundant in obese mice. Mice reproducing human metabolic exceptions displayed gut microbiota phylogenetically distinct from normal diet-fed mice, and correlated with specific adaptive immune responses. Diet composition thus has a pervasive role in co-regulating adaptive immunity and the diversity of microbiota. Frontiers Media S.A. 2017-06-22 /pmc/articles/PMC5479914/ /pubmed/28690599 http://dx.doi.org/10.3389/fmicb.2017.01157 Text en Copyright © 2017 Pindjakova, Sartini, Lo Re, Rappa, Coupe, Lelouvier, Pazienza and Vinciguerra. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Pindjakova, Jana Sartini, Claudio Lo Re, Oriana Rappa, Francesca Coupe, Berengere Lelouvier, Benjamin Pazienza, Valerio Vinciguerra, Manlio Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation |
title | Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation |
title_full | Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation |
title_fullStr | Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation |
title_full_unstemmed | Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation |
title_short | Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation |
title_sort | gut dysbiosis and adaptive immune response in diet-induced obesity vs. systemic inflammation |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479914/ https://www.ncbi.nlm.nih.gov/pubmed/28690599 http://dx.doi.org/10.3389/fmicb.2017.01157 |
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